Prostaglandin E 2 formation by rat gastroduodenal tissue following intragastric acid perfusion

Abstract

Rat gastroduodenal mucosa forms prostaglandin (PG) E 2. However, little is known about regional differences in PGE 2 formation or the effect of gastric hydrochloric acid (HCl) perfusion on regional PGE 2 formation. In this study, the rats were divided into 3 groups. Group 1 received intravenous (i.v.), 1 ml/h, and intragastric (i.g.), 8 ml/h, perfusions of saline simultaneously for 3 h. Group 2 received saline i.v. and 0.15 N HCl i.g., 8 ml/h. Group 3 was injected with a bolus of aspirin (ASA), 60 mg/kg, followed by ASA, 40 mg/kg/h i.v., and 0.15 N HCl i.g.. The gastric aspirates were analyzed for volume and pH. Segments of gastroduodenal tissue from the fundus, corpus, antrum, and duodenum were minced and then incubated in 1 ml of 50 mM Tris buffer, pH 8.4, for 30 sec with mixing; the incubate was assayed for PGE 2 by radioimmunoassay. Intragastric HCl decreased the pH of aspirate without producing gastric mucosal lesions. However, when combined with i.v. ASA, ulcer formation was present in all animals (p < 0.05). PGE 2 was formed by isolated tissue from four different gastroduodenal regions. The duodenum formed significantly greater amounts than the fundus, antrum, or corpus, which were similar. Intragastric HC1 produced a trend toward increased PGE 2 formation (pmol PGE 2/mg tissue) in the fundus, 143 ± 36 to 237 ± 57; corpus, 87 ± 13 to 200 ± 57; antrum, 157 ± 28 to 224 ± 65; and duodenum, 235 ± 56 to 338 ± 51. However, statistical significance was not reached. Intragastric HC1 combined with i.v. ASA reduced PGE 2 formation by tissue from all four regions below detectable levels. The data indicate that PGE 2α formation by rat gastroduodenal tissue differs regionally, and i.g. HCl perfusion did not significantly increase PGE 2 formation. However, when i.g. HCl perfusion combined with i.v. ASA, the PGE 2 formation was reduced below detectable levels.